Commentary|Videos|September 7, 2026

The PMOS Diagnostic Workup: Labs, Rule-Outs, and Timing Tips

Fact checked by: Sydney Jennings

Experts break down which labs actually change PMOS management and how to avoid diagnostic pitfalls.

Welcome back to this Contemporary OB/GYN, Contemporary Pediatrics, and Patient Care Online Special Report series, exploring the global consensus on renaming polycystic ovary syndrome (PCOS) to polyendocrine metabolic ovarian syndrome (PMOS). Across 5 episodes, our host and experts examine what this shift means for diagnosis, management, and patient care across the reproductive lifespan.

Our Experts:

  • Heather Appelbaum, MD, FACOG, is director of Pediatric and Adolescent Gynecology at K. Hovnanian Children's Hospital at Hackensack Meridian Jersey Shore University Medical Center. She is an associate professor of Obstetrics and Gynecology at Hackensack Meridian School of Medicine and director of the PMOS Multidisciplinary Program at Jersey Shore University Medical Center.
  • Melanie Cree, MD, PhD, is a professor of Pediatric Endocrinology at the University of Colorado Anschutz Campus and founder and director of the PMOS Multi-disciplinary Clinic at Children's Hospital Colorado. She serves on the board of the Androgen Excess PMOS Society.
  • Michelle M. Maresca, MD, is medical director for pediatric obesity medicine at Joseph M. Sanzari Children's Hospital at Hackensack Meridian Hackensack University Medical Center in New Jersey. She is a member of the pediatric and advocacy committees of the Obesity Medicine Association.

In this episode, the panel breaks down which laboratory tests actually change clinical management for PMOS, from ruling out mimics to interpreting ambiguous hormone panels.

Michelle M. Maresca, MD, walked through her diagnostic approach, beginning with ruling out mimics: Cushing syndrome (thick violaceous striae, buffalo hump, facial redness, hypertension), nonclassic congenital adrenal hyperplasia, and hypothyroidism, which can also disrupt menstrual cycles. Once PMOS is confirmed, she screens for associated metabolic complications with a lipid panel, liver function tests, blood pressure measurement, and a sleep study when obstructive sleep apnea is suspected. On insulin testing, she said fasting insulin levels rarely change management, since insulin secretion fluctuates constantly; she relies instead on HDL, triglycerides, and hemoglobin A1c, reserving a glucose tolerance test for patients borderline on A1c who could still have elevated postprandial glucose.

Melanie Cree, MD, PhD, agreed that fasting insulin is largely unhelpful and noted that across her multicenter research cohort, most sites now rely on A1c rather than oral glucose tolerance testing. Citing pediatric diabetes trial data showing that disease progresses aggressively and resists delay once A1c crosses a certain threshold, she said she keeps a low threshold for starting metformin, treating every adolescent with PMOS as functionally insulin resistant.

Both physicians flagged sex hormone binding globulin (SHBG) as a key marker: when SHBG runs low due to insulin resistance, total testosterone can appear falsely normal even though free testosterone is elevated, making a full androgen panel, rather than total testosterone alone, essential. Cree added 2 diagnostic habits outside formal guidelines: ruling out a prolactinoma and primary ovarian failure with FSH testing, and checking LH, noting that an LH level higher than FSH is common among adolescents with PMOS and can help tip ambiguous cases. Because testosterone follows a diurnal rhythm, she recommended redrawing afternoon labs the following morning. Maresca added that DHEA sulfate catches androgen elevations that testosterone alone can miss, something Cree's research has also found in a meaningful share of adolescents nationally.

In the next episode, "The Future of PMOS Care: GLP-1 Therapy and Weight-Loss Caution," the panel shares early trial data on GLP-1 therapy for PMOS and cautions the panel on how fast is too fast for adolescent weight loss.


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